The expression of nonmuscle myosin heavy chain in rat renal transplantation.
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Publications and source records attributed to J Suzuki.
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OBJECTIVES: A long-term follow-up study with nuclear magnetic resonance (NMR) imaging was undertaken to detect the morphological onset and to establish the early diagnosis in apical hypertrophic cardiomyopathy (HCM). BACKGROUND: A spadelike configuration on left ventriculogram (LVG) is regarded as a diagnostic criterion for the classical apical HCM. There also exists a segmented hypertrophy at the apical level without indicating the spadelike features (a nonspade configuration). To detect the hypertrophied myocardium of the nonspade configuration, circumferential scrutiny of the apex is required. Although both configurations can be underlying causes of giant negative T waves, etiological relationship between the two is not clarified. METHODS: The criteria for the spadelike configuration defined on left ventricular short-axis NMR images were as follows: (apical maximal thickness > or = 15 mm), (apical anterior thickness over basal anterior thickness > or = 1.3) and (apical posterior thickness over basal posterior thickness > or =1.3). Thirteen patients who had predominant hypertrophy (> or = 15 mm) at the apical level without the spadelike configuration underwent NMR imaging twice before and after 54+/-10 months' follow-up. RESULTS: Apical hypertrophy that had been confined to the lateral wall in four, the anterior-lateral wall in two, and the septal-anterior wall in one developed to become circumferential hypertrophy that fulfilled the criteria for the spadelike configuration after the follow-up period. CONCLUSIONS: The spadelike configuration can begin with the nonspade configuration and therefore, both can constitute a single disease entity of apical HCM. The early diagnosis of apical HCM can be achieved by identifying the hypertrophy frequently confined to the lateral wall at the apical level.
In this study, we examined the effect of serial extraction alone on crowding. We also investigated the relationships between tooth width, arch length, and irregularity index. Maxillary dental casts from 32 subjects who had undergone only serial extraction were analyzed at 3 stages: before deciduous canines extraction, after first premolars extraction, and at the end of the observation period. The mean of the irregularity index decreased significantly as serial extraction proceeded and further decreased during the observation period. In cases where the width of the incisor was more than 2 standard deviations above the means for the control subjects, there was a significant correlation between tooth width of the lateral incisors and irregularity index before extraction as well as a significant correlation between the summation of tooth widths of the central and lateral incisors and irregularity index at that time. There was a significant negative correlation between arch length discrepancy and irregularity index before extraction and also a significant correlation between arch length discrepancy and correction of the irregularity index from before deciduous canines extraction to after first premolars extraction. These results suggest that tooth width and arch length discrepancy might preferentially affect the degree of anterior crowding in cases of severe crowding. There was no aggravation of the average crowding level during the observation period in the present study. The present study quantitatively suggested that serial extraction was useful for the purpose of correcting crowding in most cases.
Administration of anti-intercellular adhesion molecule (ICAM)-1 monoclonal antibody (mAb) plus anti-lymphocyte function associated antigen (LFA)-1 mAb induces tolerance in murine cardiac transplantation, while anti-vascular cell adhesion molecule (VCAM)-1 mAb plus anti-very late antigen (VLA)-4 mAb administration prolongs graft survival, but leads to tolerance only in some cases. BALB/c mice hearts were transplanted into C3H/He recipients. Each combination of anti-VCAM-1 plus anti-VLA-4 mAbs (100 microg each/day, i.p.) or anti-ICAM-1 plus anti-LFA-1 mAbs (50 microg each/day, i.p.) was administered for 5 days. For control study, third group mice received daily with FK506 administration (1 mg/kg/day). The cardiac allografts and recipients' spleens were harvested on day 7; the expression of cytokines were detected using immunohistochemistry, reverse transcription-polymerase chain reaction (RT-PCR) and in situ RT-PCR. Th2 cytokines (IL-4 and IL-10) were markedly enhanced and Th1 cytokines (IFN-gamma and IL-2) were suppressed in recipients treated with anti-ICAM-1 mAb plus anti-LFA-1 mAb, while poor Th2 cytokine expression allowed persistent Th1 cytokine expression in recipient mice with anti-VCAM-1 mAb plus anti-VLA-4 mAb treatment. Both Th1 and Th2 cytokine expression was suppressed in FK506-treated mice. It is concluded that immunological tolerance and prolonged graft survival induced by blocking cell adhesion is regulated by different cytokine expression.
It has been suggested that the 65 kDa heat-shock protein (HSP) of Streptococcus in recurrent aphthae within the oral cavity may be involved in the uveoretinitis of Behçet's disease, possibly through sensitization of the immune system. To investigate this possibility, we examined serum antibody titers for various members of the 60 kDa family of HSPs and their implications with regard to a role for HSP60s in Behçet's disease. We isolated HSP60 of Streptococcus pyogenes from the margin of oral aphthae in one Behçet's disease patient with severe uveoretinitis and the HSP60s of Yersinia enterocolitica, retinoblastoma cell line clone Y79, and bovine retinal extract and investigated the reaction of each of these HSP60s with 100-fold diluted serum samples from 20 Behçet's disease patients using anti-HSP60 antibody titers determined by ELISA. The anti- Streptococcus HSP60 antibody and anti-retinal HSP60 antibody titers of the 100-fold diluted serum samples from the Behçet's disease patients were both significantly higher than those of similarly diluted serum samples from healthy donors. The results of the ELISA antibody titer assay showed that, although the various HSP60s share a common basic antigenicity, they differed in reactivity to the anti-HSP60 antibodies in the sera of the Behçet's disease patients. The results indicate that subtle but significant differences exist in the antigenicity of the various HSP60s tested, all of which share a common basic antigenicity and are of approximately the same molecular weight, and suggest that an immuno-cross-reaction between retinal and streptococcal HSPs and a related autoimmune response may be involved in the development of Behçet's disease.
It is well known that G-rich phosphorothioate oligonucleotides (G-rich PS) bind to the V3 loop of HIV-1 gp120 and inhibit HIV-1 infection. In this study, we investigated the inhibitory mechanism of a new type of G-rich PS (PS-G3T4G3) on the replication cycle of HIV-1. PS-G3T4G3 inhibits both cell to cell and cell free infections. Binding and entry assays revealed that the inhibitory step of PS-G3T4G3 occurs at the early stage of HIV-1 infection. V3 loop-specific mAb test showed that PS-G3T4G3 binds to the V3 loop and prevents its interaction with chemokine receptors. These results suggest that PS-G3T4G3 may be a novel candidate for an HIV-1 inhibitor.
Tetraspans transmembrane family (TSTF) members, also known as tetraspanin superfamily, have various effects on cell proliferation, motility, and adhesion not only in hematopoietic cells, but also in other type of cells. However, little is known about their expression in the human gastrointestinal (GI) tract. The authors characterized immunohistologically the localization of six members of TSTF (CD9, CD37, CD53, CD63, CD81, and CD82) in the normal epithelium from esophagus to colon. CD9 and CD82 molecules were strongly expressed in all epithelial surface membranes, from esophagus to colon, and their staining pattern was quite similar. Expression of CD37 was not detectable throughout the GI tract. Expression of CD53 was barely detectable. Expression of CD63 was clearly detected distal to the stomach, including the duodenum, small intestine, and colon. On the contrary, expression of CD81 was detected only in the esophagus--confined to a few layers from the basal layer. From these data it seems likely that the expression of TSTF molecules might be regulated differentially depending on the site of the GI tract.
Increased levels of plasma catecholamine lead to cardiac hypertrophy via the alpha-, beta-adrenergic receptors, and partially, type 1 angiotensin II (AT1) receptor. However, it remains unclear whether other factors are involved in catecholamine-induced cardiac hypertrophy. We investigated the expression of insulin-like growth factor (IGF)-I in hearts of male Wistar rats infused with a beta-adrenergic agent, isoproterenol (ISO) (3 mg/kg/day), with or without an AT1-receptor antagonist, TCV-116 (10 mg/kg/day). Cardiac myocytes became hypertrophied 1 day after the beginning of ISO administration. ISO induced a biphasic increase of cardiac myocytes positive for IGF-I protein in the early and late phases of the study period, whereas IGF-I gene expression was upregulated only in the late phase by ISO. TCV- 116 abolished the upregulation of IGF-I gene and protein expression in the late phase in association with the regression of cardiac hypertrophy. These results suggest that ISO-induced cardiac hypertrophy is mediated, at least in part, by IGF-I, the expression of which is upregulated through the activation of AT1 receptor.
The purpose of this study was to investigate the intrafamilial distribution of mutans streptococci in Japanese families using chromosomal DNA fingerprinting with three endonucleases; EcoRI, HindIII and HaeIII. The analysis of 1,908 isolates cultured from the dental plaque of 76 subjects from 20 families (20 married couples and 36 of their children) resulted in the identification of 144 genotypes containing 114 strains of Streptococcus mutans (serotype c, 66.7%; e, 12.5%) and 30 strains of S. sobrinus (d, 13.2%; g, 7.6%). A mean of 1.89 genotypes (from one to four) was harbored in individual subjects, and a mean of 4.10 genotypes from two to seven was harbored in individual families. Among the 70 genotypes found in the children, 36 (51.4%) were in agreement with their mothers and 22 (31.4%) were in agreement with their fathers. The other genotypes (18.6%) did not correspond with the parents. Homologous strains between parents were found in only two couples. This result showed that fathers or others as well as mothers can be sources of transmission. Further, the serotype d, e and g strains showed significantly higher probabilities of transmission than serotype c.
PCR-restriction fragment length polymorphism electrophoretic patterns of amplified ureB and ureC of Helicobacter pylori were compared between spouses after digestion with restriction endonucleases. Twenty of 21 couples, both members of which were positive for H. pylori, showed ureB and ureC patterns that differed between spouses. We concluded that in Japan, interspousal transmission of H. pylori occurs rarely.
The dissociating and/or residual inhibitory effects of bopindolol from beta-adrenoceptors (ARs) of atria strips pretreated with this drug and washed out with buffers on isoprenaline-induced chronotropic actions were determined. The effects of this drug were compared with those of its active metabolite 18-502, propranolol, and pindolol. Our results are as follows: (1) Lower concentrations of bopindolol (10(-9) and 10(-8) mol/l) and the active metabolite 18-502 (10(-9) mol/l), propranolol (10(-8) and 10(-6) mol/l) and pindolol (10(-8) mol/l) produced rightward shifts of concentration-response curves of isoprenaline. (2) Higher concentrations of bopindolol (10(-7) mol/l) and 18-502 (10(-8) and 10(-7) mol/l) produced a reduced maximum response by isoprenaline. (3) Bopindolol (10(-9)-10(-7) mol/l), 18-502 (10(-9)-10(-7) mol/l) and propranolol (10(-7) and 10(-6) mol/l) did not recover to control levels at 180 min even after washout with buffers. In conclusion, bopindolol and 18-502 may slowly dissociate and act as noncompetitive beta-antagonists rather than readily reversible beta-AR antagonists. These effects may differ from those of propranolol and pindolol, although propranolol did not recover to control levels after washout with buffer.
In Japanese patients idiopathic tubular proteinuria presents mainly as asymptomatic tubular low molecular weight proteinuria. This disease has recently been shown to resemble Dent's disease which is characterized by tubular proteinuria, hypercalciuria, rickets and eventual renal failure. We report on 4 children with idiopathic tubular proteinuria. Although they had normal renal function, as evidenced by serum creatinine or creatinine clearance, they had very poor renal accumulation of 99mTc-DMSA and the presence of large amounts of tracer in the bladder. Additionally, the patient with the largest amounts of tubular proteinuria had the poorest renal accumulation of the 4 patients. The renal accumulation of tracer decreased with time from a maximum at 10 min after injection. These findings demonstrate that the tracer, once taken to be confined to the proximal tubular cells, is immediately excreted to the tubular lumen. We suggest that poor renal accumulation of 99mTc-DMSA is very important in elucidating the mechanism of idiopathic tubular proteinuria, and that 99mTc-DMSA renoscintigraphy is useful in the evaluation of the patient's renal function over time.
BACKGROUND: L-selectin (CD62L) and Mac-1 (CD11b/CD18) play a crucial role in the infiltration of eosinophils. However, changes in CD62L and CD11b expression on eosinophils after stimulation with cytokines were little studied. METHODS: Eosinophils in peripheral blood of healthy volunteers were purified and cultured with interleukin-5 (IL-5), granulocyte/macrophage colony-stimulating factor (GM-CSF) or interferon-gamma (IFN-gamma). After up to 24 h incubation, CD62L and CD11b expression were examined using flow cytometry. The effects of dexamethasone (Dex), cycloheximide (CHX) or theophylline on CD62L expression on IFN-gamma-stimulated eosinophils were also studied. RESULTS: IL-5 or GM-CSF downregulated CD62L and upregulated CD11b expression on eosinophils after 30 min stimulation. Conversely, IFN-gamma upregulated CD62L after 12 h stimulation in a time- and dose-dependent manner, and had no effect on CD11b expression. Dex, CHX or theophylline dose-dependently decreased CD62L expression on IFN-gamma-stimulated eosinophils. CONCLUSIONS: IFN-gamma is a particular cytokine which can increase CD62L expression on circulating or infiltrated human eosinophils. It is suggested that protein synthesis and intracellular cAMP participate in the increase in L-selectin expression on IFN-gamma-stimulated eosinophils.
We evaluated abdominal muscle contractility and fatigue by measuring twitch gastric pressure (Pgat) after percutaneous supramaximal electrical stimulation of the abdominal wall before and after sit-ups to task failure. Mouth pressures during maximal voluntary expulsive maneuvers (PEmax) at TLC and FRC with superimposed twitches, and maximum voluntary ventilation (MVV) were also assessed. Mean fresh Pgat was 36.1 +/- 3.0 cm H2O with a coefficient of variation that ranged between 3.0 to 4.8%. Pgat decreased by 25% (p < 0.001) and 37% (p < 0.001) at 1 and 30 min after sit-ups. During maximal voluntary contraction twitch occlusion never occurred. PEmax at TLC and FRC decreased by 15% (p < 0.001) and 11% (p < 0.017) at 1 min, and 8% (p < 0.036) and 9% (p < 0.030) at 30 min after sit-ups, respectively. Despite the abdominal muscle fatigue, MVV values at 1 and 30 min after sit-ups were not significantly different from the value obtained before the sit-ups. We conclude that (1) Pgat is a useful objective indicator of abdominal muscle contractility and fatigue; (2) during maximal voluntary expulsive maneuvers the abdominal muscles are never fully activated; (3) sit-ups lead to substantial low-frequency fatigue but little high-frequency fatigue of the abdominal muscles, which has little effect on maximal breathing capacity.
For the early detection of myocardial damage associated with anthracycline therapy, electrocardiography, echocardiography, and radionuclide angiocardiography were used to assess cardiac function in 37 patients receiving anthracyclines (ie, adriamycin and daunorubicin at a total dose of 100-2,030 mg/m2). None of the patients developed clinical congestive heart failure. There were no significant changes of electrocardiographic and echocardiographic parameters after anthracycline administration. The left ventricular ejection fraction did not change significantly on radionuclide angiocardiography. However, the 1/3 peak filling rate (PFR) corrected by the end-diastolic count (EDC) (1/3 PFR/EDC) and the 1/3 filling fraction (1/3 FF), the indices of early diastolic function, showed a significant decrease. These findings suggest that the 1/3 PFR/EDC and 1/3 FF determined by radionuclide imaging are useful for detecting silent myocardial damage induced by anthracyclines.
A report is presented of a liquefaction necrosis of mitral annular calcification in a patient with chronic renal failure and secondary hyperparathyroidism who had been managed by hemodialysis for 11 years. The mass was echogenic with an echo-lucent area inside, high density on computed tomography and low intensity on magnetic resonance imaging. The uptake of gallium-67 (67Ga)-citrate and the bone agent technetium-99m-methylene diphosphate (99mTc-MDP) was seen in the mass. These findings were compatible with liquefaction necrosis of the mitral annular calcification. After treatment with low calcium concentration hemodialysis, the size of the mass reduced with disappearance of the echo-lucent area on the echocardiography and there was no uptake of 67Ga-citrate or 99mTc-MDP. Liquefaction necrosis might be the early and reversible form of mitral annular calcification. When a tumorlike echogenic mass at the base of mitral leaflets is seen in patients with predisposing factors for mitral annular calcification, consider the possibility of this specific form of mitral annular calcification in order to avoid any unnecessary surgical intervention.
Multivessel spasm in variant angina is believed to be a major prognostic factor. Three patterns of multivessel spasm have been detected: (1) spasm at different sites on different occasions (migratory spasm); (2) spasm sequentially affecting 2 different sites (sequential spasm); and (3) simultaneous spasm at more than 1 site (simultaneous spasm). The present study investigated the prognosis based on this factor for variant angina without fixed coronary stenosis and examined the influence of multivessel spasm on cardiac events. Twenty-six patients were diagnosed as having variant angina without fixed coronary stenosis using 12-lead 24-h ECG recording system and coronary cineangiography. These patients were followed up prospectively for 57.1+/-7.6 months. Of the 26 patients 13 had single-vessel spasm, 6 had migratory multivessel spasm angina, and 7 showed sequential and/or simultaneous multivessel spasm angina. The survival free of serious cardiac events and of all cardiac events was significantly lower for patients with sequential and/or simultaneous multivessel spasm than for those with migratory multivessel spasm (p<0.05, p<0.05), whereas for patients with migratory multivessel spasm the difference comparison with single-vessel spasm did not attain statistical significance (p = ns, p = ns). The results of this study suggest that there seems to be a high-risk subgroup (i.e., sequential and/or simultaneous multivessel spasm) among patients with variant angina.
A 56-year-old man presented with an inferior myocardial infarction and a huge pseudoaneurysm below the inferior surface of the left ventricle, which had progressed from a small subepicardial aneurysm over a 6-month period. Transthoracic echocardiography, Doppler color flow images, radionuclide angiocardiography, magnetic resonance imaging and contrast ventriculography all revealed an abrupt disruption of the myocardium at the neck of the pseudoaneurysm, where the diameter of the orifice was smaller than the aneurysm itself, and abnormal blood flows from the left ventricle to the cavity through the orifice with an expansion of the cavity in systole and from the cavity to the left ventricle with the deflation of the cavity in diastole. Coronary angiography revealed 99% stenosis at the atrioventricular nodal branch of the right coronary artery. At surgery the pericardium was adherent to the aneurysmal wall and a 1.5-cm orifice between the aneurysm and the left ventricle was seen. Pathological examination revealed no myocardial elements in the aneurysmal wall. The orifice was closed and the postoperative course was uneventful. Over-intense physical activity as a construction worker was considered to be the cause of the large pseudoaneurysm developing from the subepicardial aneurysm. These findings indicate that a subepicardial aneurysm may progress to a larger pseudoaneurysm, which has a propensity to rupture, however, it can be surgically repaired.